Microbial Diseases of the Skin and Wounds Notes

Rockeem's Acne: A Case Study

  • Rockeem, a 13-year-old, is distressed by severe acne on his face, neck, and back.
  • He's self-conscious and worried about the cause, questioning diet and hygiene.
  • His mother schedules an appointment with a dermatologist.

Skin Structure (Layers and Functions)

  • The skin, also known as the cutaneous membrane, is a flexible and tough membrane.
  • It prevents excessive water loss and regulates body temperature through sweat production and blood vessel dilation/constriction.
  • It also helps in the formation of vitamin D and is involved in sensory phenomena.
  • Skin is a significant barrier against microbial invaders due to its physical and chemical properties, limiting infection and disease unless wounded.
  • The skin covers about 2 square meters in an adult.
  • Skin thickness ranges from 0.05 mm on the lips to 4.0 mm on the soles of the feet, and in calluses.
  • Skin is composed of two layers: the deeper dermis and the superficial epidermis. The dermis is a tough, leathery structure
    with loosely packed cells, protein fibers, small muscles, sweat glands, sebaceous (oil) glands, blood vessels, nerve endings, and hair follicles.
  • The dermis provides strength and flexibility and supports the epidermis.
  • The epidermis consists of four to five layers of tightly packed cells.
  • Basal cells of the epidermis adjoin the dermis and divide continuously.
  • As daughter cells are pushed toward the surface, they flatten and die after absorbing melanin, a pigment that gives skin its color.
  • Epidermal cells fill with keratin, a waterproofing protein. A hardened form of keratin forms nails and hairs, which are accessory structures to the skin.
  • Dendritic cells phagocytize microbes that penetrate the deeper layers of the epidermis and deliver microbial antigens to defensive lymphocytes.
  • The skin surface is generally inhospitable, covered with salt from sweat and sebum, an oily lipid secreted by sebaceous glands in the dermis.
  • Chemicals in sweat and sebum are antimicrobial.
  • The outermost layer of skin consists of flattened, dead, dry, keratinized cells covered with oil and salt, acting as a barrier to microbial invasion.
  • The skin sloughs off microbes attached to the outermost skin flakes as epidermal cells are continually pushed upwards, replacing the outer layers monthly.
  • The hypodermis, a layer of fat cells and fibers, lies beneath the dermis and is subcutaneous.
  • It provides cushioning, insulation, and a ready energy source and anchors the skin to the underlying tissues.
  • Wounds are trauma to any tissue of the body, such as cuts, abrasions, burns, or surgery, breaching the mechanical barrier and allowing microbes to infect deeper tissues.
  • Microbes within a wound can multiply and produce enzymes and toxins, detrimental to the host. The body starts to heal a wound by forming a blood clot.
  • Neighboring connective and epithelial cells multiply and grow into the clot. Body defenses, including phagocytosis, complement and inflammation, eliminate infection.
  • Some infections overwhelm the body’s defenses, resulting in severe or fatal diseases.

Normal Microbiota of the Skin

  • Some yeasts and bacteria thrive in the harsh conditions of the epidermis, hair follicles, and sweat ducts.
  • These harmless residents make up the microbiota, competing with potential pathogens for nutrients and producing chemicals that interfere with their growth.
  • Vigorous scrubbing may reduce but not eliminate them completely.
  • Microbiota typically grow in small clusters, particularly in moist areas such as armpits, producing body odor.
  • Significant members of the microbiota include lipophilic yeasts like Malassezia.
  • Aerobic, Gram-positive bacteria in the genera Staphylococcus and Micrococcus also grow on the skin.
  • These bacteria can tolerate salt concentrations of 5–10%.
  • The most common species is Staphylococcus epidermidis.
  • Diphtheroids are another common type of Gram-positive bacterial microbiota that includes Propionibacterium acnes.
  • P. acnes resides in hair follicles and ferments carbohydrates to form propionic acid, which lowers the pH of the skin, defending against infection.
  • Pathogenic microbes can still produce diseases by penetrating the epidermis through wounds or when the immune system is suppressed.
  • Bacteria, viruses, fungi, protozoa, and arthropods are involved in skin diseases, and diseases of other body systems may also manifest themselves in the skin.

Bacterial Diseases of the Skin

  • Bacterial infections range from mild acne to life-threatening infections, with bacteria infecting the skin including Staphylococcus, Streptococcus, Propionibacterium, Bartonella, Pseudomonas, and Rickettsia.

Staphylococcus Virulence Factors

  • Staphylococci exhibit enzymes, structures to evade phagocytosis, and toxins that allows them to produce diseases.
  • Virulent S. aureus strains produce several enzymes:
    • Coagulase clots blood, hiding the bacterium from phagocytes.
    • Hyaluronidase breaks down hyaluronic acid, enabling spread between cells.
    • Staphylokinase dissolves blood clots, allowing spread to new locations.
    • Lipases digest lipids, providing staphylococci with food on the surface of skin, in hair follicles, and in sebaceous glands.
    • β-Lactamase conveys resistance to beta-lactam antimicrobial drugs.
  • Structural defenses against phagocytosis:
    • Both S. aureus and S. epidermidis synthesize polysaccharide slime layers/capsules that inhibit chemotaxis and phagocytosis by leukocytes.
    • The slime layer facilitates attachment of staphylococcal biofilms to artificial surfaces, such as catheters.
    • S. aureus cells are coated with protein A, which binds to the stems of class G antibodies (IgG), inhibiting opsonization and triggering of the complement cascade.
  • Toxins: Pathogenic S. aureus possesses several toxins that contribute to virulence:
    • Cytolytic toxins disrupt the cytoplasmic membranes of a variety of cells.
    • Leukocidin kills leukocytes, providing Staphylococcus with additional protection against phagocytosis.
    • Epidermal cell differentiation inhibitor induces large holes in the linings of blood vessels, allowing access for the bacterium to invade tissues.
    • Exfoliative toxin and toxic shock syndrome toxin may cause staphylococcal scalded skin syndrome and staphylococcal toxic shock syndrome.

Folliculitis

  • Folliculitis is an infection of a hair follicle, often called a pimple.
  • When it occurs at the base of an eyelid, it is called a sty.
  • A furuncle (boil) is a large, painful nodular extension of folliculitis resulting from spread of the infection into surrounding tissues.
  • A carbuncle results when several furuncles join together, more frequently in areas where the skin is thick.
  • In severe cases, the body triggers fever in response to folliculitis.

Staphylococcus

  • Staphylococcus is the most common cause of folliculitis and associated infections of the skin and upper respiratory tract.
  • Staphylococci cells are salt tolerant, capable of growing in media containing up to 10% NaCl, explaining how they tolerate the salty surface of human skin.
  • Salt tolerance, drying out, solar radiation, and heat (up to 60°C for 30 min) allows Staphylococcus to survive on environmental surfaces in addition to skin.

Staphylococcal Scalded Skin Syndrome (SSSS)

  • Five percent of S. aureus strains secrete exfoliative toxins, leading to separation of outer epidermis cells.
  • SSSS involves reddening/wrinkling of skin near the mouth, spreading to the entire body, followed by blisters containing clear fluid. Affected epidermis peels off in sheets within two days.

Impetigo (Pyoderma) and Erysipelas

  • Impetigo, also called pyoderma, is a contagious disease characterized by small, flattened, red patches that appear primarily on the face and limbs.
    • Patches develop into oozing, pus-filled vesicles, which eventually break and form a thick honey-colored, sticky crust (intense itching).
    • Numerous vesicles are at various stages of development because bacteria from a vesicle spread to adjacent sites on the skin.
  • Erysipelas is when the skin infection spreads into surrounding lymph nodes, triggers pain/inflammation (reddening of the skin on the face, arms, or legs).
    • The red area has a distinct margin. Also causes swollen local lymph nodes, pain, fever, chills, and leukocytosis.
    • Without treatment, erysipelas may be fatal, with mortality ranging from 2% to 17% (very young, old, and immunocompromised are more likely to die).

Impetigo and Erysipelas Pathogens and Virulence Factors

  • S. aureus alone causes about 80% of impetigo cases, about 20% involve Streptococcus pyogenes alone or in conjunction with S. aureus.
  • S. pyogenes, synonymously called group A Streptococcus, is a Gram-positive coccus whose offspring in chains following cell division and causes erysipelas.

Necrotizing Fasciitis

  • Most patients initially report a hot, intensely painful, sunburn-like rash at the site of infection, then several bacteria can cause necrotizing fasciitis.
  • The most common cause is Streptococcus pyogenes, also known as group A Streptococcus.
  • Group A Streptococcus is transmitted to another person through breaks in the skin. Necrotizing fasciitis has been developed following insect bite or a needlestick to draw blood.

Acne

  • The common causes of Propionibacteria, small, Gram-positive, rod-shaped diphtheroids Propionibacterium acnes causes acne in 85% of afflicted adolescents and young adults.
  • Propionibacterium typically grows on sebum within the sebaceous glands of the skin. Excessive oil production triggered by adolescence hormones stimulates the growth of the bacteria.
  • The bacteria secrete chemicals that attract leukocytes and trigger inflammation (leukocytes phagocytize and release chemicals causing local inflammation).
  • A blackhead is formed when a plug of dead and dying bacteria blocks the pore.
  • In cystic acne, a severe form, bacteria form cyst which rupture, and triggering the formation of scar tissue. Acne typically develops on skin with sebaceous glands.

Cat Scratch Disease

  • Caused by Bartonella henselae (Gram-negative aerobic bacillus). Primary virulence factor is endotoxin (lipid A) in the outer membrane of Gram-negative bacteria. Grows/reproduces inside red blood cells/cells lining blood vessel walls.
  • Pathogenesis and Epidemiology is that Cat Scratches/bites introduce the bacterium into the skin. In skin, the bacterium grows intracellularly, releasing endotoxin when it dies triggers fever and blood clotting.
  • Diagnosis by positive indirect fluorescent antibody test. Treatment by Rifampin, ciprofloxacin or gentamicin, and prevention is avoidance of cat-inflicted wounds/adequate cleansing of wounds.

Pseudomonas Infection

  • Symptoms include fever, chills, shock and Blue-green pigment produced.
  • Virulence Factors for Pseudomonas include Fimbriae, and adhesins.
  • Forms capsule, Neuraminidase, Elastase.

Spotted Fever Rickettsiosis

  • Rocky Mountain spotted fever (RMSF) manifests with a spotted rash and sudden fever, headache.
  • The tick transmits pathogens among humans and rodents acting as reservoirs
  • Diagnosis from a rash and headache is confirmed with antibody stains and treatment with doxycycline or chloramphenicol

Cutaneous Anthrax

  • Cutaneous Anthrax results when bacillus anthracis endospores enter a cut in the skin
  • Physicians can treat cutaneous anthrax effectively with multiple prescribed drugs. Requires control of the disease in animals.

Gas Gangrene

  • Clostridium produce toxins which kill surrounding tissues, providing nutrients for the bacteria to grow
  • Diagnosis comes from the appearance. The condition is a medical emergency requiring removal of dead tissue combined with aggressive administration.

Viral Diseases of the Skin

  • Smallpox produces lesions that progress through stages such as macule and pustule
    • Vaccination campaigns have eradicated such diseases in nature
    • Herpes manifests as recurring blisters on the genitalia and is caused by infections with the human herpes virus and often has no visible symptoms.

Fungal Diseases of the Hair, Nails, and Skin

  • Surface Mycoses is characterized by hyperpigmented patches on the skin from fungal interference of melanin production such can be acquired via direct contact and treated with antifungal solutions

Other Terms Reviewed:

  • The dermis is covered by a superficial (outer) epidermis

  • The surface of the skin is a generally inhospitable environment covered with salt (left behind as sweat evaporates) and sebum

  • The hypodermis is a layer of fat cells and fibers lying beneath the dermis. It is not technically part of the skin; it is subcutaneous. Wounds are trauma to any tissue of the body. Cuts, abrasions, scrapes, surgery, inoculations, bites, and other penetrating skin wounds, as well as burns, breach the significant mechanical barrier provided by intact epidermis and dermis, allowing microbes to infect the warm, moist, deeper tissues of the body.

  • The microbiota compete with potential pathogens for nutrients and space and produce chemicals that interfere with the growth of other microbes, providing further defense against infection.

  • It is critical to clean and drain abscesses of pus for subsequent topical antibiotic therapy with mupirocin to be effective, to prevent MRSA.

  • Staphylococcal Scalded Skin Syndrome is primarily disease of infants and children. To prevent, consider diseases caused by Staphylococcus acting alone. Then we turn our attention to diseases of Streptococcus acting alone or in conjunction with Staphylococcus.

  • Antibacterial drugs Rifampicin, ciprofloxacin, or gentamicin treat cat scratch diseases. This examines a potential positive role for Bartonella on vessels made from scratch.

  • Pseudomonas Aeruginosa is an opportunistic pathogen of burn victims, to prevent, treatment of cutaneous anthrax with oral antimicrobial drugs such as ciprofloxacin, penicillin, or erythromycin for 60 days.